Project description:To assess the role of LSD1 in mouse small intestinal epithelium, we grew small intestinal organoids in vitro from mice with an epithelial specific deletion of LSD1 (Villin-Cre+; Lsd1f/f) and from wild type (Villin-Cre-; Lsd1f/f) mice. This experiment uses a new Cre strain with 100% recombination efficiency. Similar to intestinal epithelium from mice with an intestinal epithelium specific LSD1-KO, Paneth cells are not present in LSD1-KO small intestinal organoids. We used these sequencing data to show intrinsic epithelial changes in the intestinal epithelium caused by LSD1 deletion in the absence of microbiota and surrounding in vivo cell types.
Project description:Gene expression in the colonic mucosa of wild-type and p38a-knockout intestinal epithelial cells (IECs) were compared. C57BL/6 wild-type mice, and intestinal epithelial cell-specific p38a-knockout mice on a C57BL/6 background were used for isolation of colonic mucosa
Project description:Mice with an intestinal epithelial specific knockout of LSD1 have changes in the intestinal epithelium including loss of Paneth and Goblet cells along with a general status of epithelial immaturity. To assess the influence of these epithelial specific changes on the mucosal immune system we performed a scRNAseq on CD45+ immune cells from the small intestine of mice with an epithelial specific LSD1 deletion (Villin-Cre+; Lsd1f/f) and wild type mice (Villin-Cre -; Lsd1f/f). To rule out a possible influence of the bacterial microbiome in the observed changes in CD45+ cell types we performed the same experiment in mice treated with antibiotics. These data allowed us to pinpoint changes in the cell populations of the mucosal immune system upon loss of LSD1 in the intestinal epithelium such as IgA producing cells and ILCs.
Project description:Transcription profiling by array of intestinal epithelial cells (IECs) in germ-free conditions from mice with IEC-specific HDAC3 deletion against wild type controls
Project description:The aim of this study is to compare the transcriptomic profile of colonic intestinal epithelial cells (IECs) at steady-state, and in several models of colitis: in naive wild-type C57BL/6 mice, in wild-type C57BL/6 mice treated for 7 days with 3% dextran sodium sulfate (DSS) in drinking water, in Il10-/- C57BL/6 mice and Il10-/- C57BL/6 mice with IEC-specific Rabgef1 deletion. Colonic IECs were isolated and FACS-sorted, then subjected tu bulk RNA-seq.
Project description:Mice lacking 3-hydroxy-3-methylglutaryl-coenzyme A reductase (Hmgcr) in intestinal villus and crypt epithelial cells were generated using a Villin-Cre transgene. Label free proteome profiling was measure for Wild type and KO mouse.
Project description:The intestinal epithelium is a complex, constitutively renewing tissue composed of functionally distinct intestinal epithelial cells (IECs), whose specific cell fates are established and maintained through cell-specific activity of transcription factors, as well as precise gene silencing by chromatin compaction. By facilitating chromatin condensation through histone modification, SETDB1, a histone-lysine N-methyltransferase, is one of the central factors involved in regulation of epigenetic transcriptional repression. Therefore, we set out to study the potential roles of SETDB1 in intestinal epithelial homeostasis and inflammatory bowel disease (IBD). We used RNA-sequencing to profile gene expression changes in intestinal epithelial cells of mice with tamoxifen (TAM)-inducible (Villin-CreERT2) IEC-specific deletion of Setdb1 on day 2 post TAM-injection start, compared to TAM-treated wild-type littermates. We find an expression profile which indicates intestinal epithelial cell death and induction of type I interferon signaling, as a result of de-repression of endogenous retroviruses.
Project description:We compared gene expression profile of jejunum crypt samples of Sox9 deficient mice and wild type control mice in order to identify the genes that are regulated by SOX9 in the small intestinal crypt epithelial cells. The intestinal epithelial cells were collected from crypts of jejunum of three 3-mo-old Sox9 mutant mice and three littermate controls.
Project description:Gene expression in the colonic mucosa of wild-type and p38a-knockout intestinal epithelial cells (IECs) were compared. C57BL/6 wild-type mice, and intestinal epithelial cell-specific p38a-knockout mice on a C57BL/6 background were used for isolation of colonic mucosa Gene expression in each genotype was analyzed in triplicate.
Project description:Caspase-8 is a cystein protease involved in regulating apoptosis. The function of caspase-8 was studied in the intestinal epithelium, using mice with an intestinal epithelial cell specific deletion of caspase-8. We used microarrays to investigate the difference of the global programme of gene expression in intestinal epithelial cells of control and caspase-8 deficient mice. Intestinal epithelial cells were isolated from 3 control mice and 3 mice with a conditional deletion of caspase-8 in the intestinal epithelium. RNA was isolated and subjected to Affymetrix gene chip analysis.